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      Nuevas estrategias en el tratamiento del síndrome antifosfolípido Translated title: New alternatives for the treatment of antiphospholipid syndrome. A literature review

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          Translated abstract

          For years the mainstay of antiphospholipid syndrome treatment has been anticoagulation and antiplatelet therapy, but the autoimmune nature of the disease, and complications of these therapies, created the need to develop new therapeutic strategies. New therapeutic alternatives inhibit at different levels, the cascade of events leading to the pro-thrombotic state characteristic of the antiphospholipid syndrome. We conducted a literature review of these new treatments, focusing on the pathophysiological bases that support them and their possible clinical applications.

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          The antiphospholipid syndrome.

          Jerrold S Levine, D Ware Branch, Joyce Rauch (2002)
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            Hydroxychloroquine directly reduces the binding of antiphospholipid antibody-beta2-glycoprotein I complexes to phospholipid bilayers.

            S. Quinn, Jacob Rand, Douglas Taatjes … (2008)
            Treatment with the antimalarial drug hydroxychloroquine (HCQ) has been associated with reduced risk of thrombosis in the antiphospholipid (aPL) syndrome (APS) and, in an animal model of APS, with reduction of experimentally induced thrombosis. Recognition of beta2-glycoprotein I (beta2GPI) by aPL antibodies appears to play a major role in the disease process. We therefore used the techniques of ellipsometry and atomic force microscopy (AFM) to investigate whether HCQ directly affects the formation of aPL IgG-beta2GPI complexes on phospholipid bilayers. HCQ, at concentrations of 1 mug/mL and greater, significantly reduced the binding of aPL-beta2GPI complexes to phospholipid surfaces and THP-1 (human acute monocytic leukemia cell line) monocytes. The drug also reduced the binding of the individual proteins to bilayers. This HCQ-mediated reduction of binding was completely reversed when the HCQ-protein solutions were dialyzed against buffer. HCQ also caused modest, but statistically significant, reductions of clinical antiphospholipid assays. In conclusion, HCQ reduces the formation of aPL-beta2GPI complexes to phospholipid bilayers and cells. This effect appears to be due to reversible interactions between HCQ and the proteins and may contribute to the observed reduction of thrombosis in human and experimental APS. These results support the possibility that HCQ, or analogous molecules, may offer novel nonanticoagulant therapeutic strategies for treating APS.
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              Hydroxychloroquine reverses thrombogenic properties of antiphospholipid antibodies in mice.

              Keith J. Edwards, Silvia Pierangeli, Daniel Anderson … (1997)
              Previous studies have demonstrated that human monoclonal and polyclonal anticardiolipin antibodies have thrombogenic properties in vivo. Using such a model in which these antibodies have been shown to increase both the size of an induced thrombus and the duration of time in which such a clot lasts, we investigated whether hydroxychloroquine alters the dynamics of such thrombus formation. Three groups of nine mice were injected with purified immunoglobulin G (IgG) from a patient with the antiphospholipid syndrome (IgG-APS) and then fed with hydroxychloroquine at various doses (100, 6, and 3 mg/kg body wt). Three control groups of mice were also studied, including mice injected with IgG-APS and then fed with placebo, as well as two other groups injected with IgG from normal human serum and fed either hydroxychloroquine or placebo. A standardized thrombogenic injury was subsequently induced in the femoral vein of each mouse and the area (size) of thrombus measured as well as the total period of time that thrombus was present. Mice treated with hydroxychloroquine and IgG-APS showed significantly smaller thrombi that persisted for a shorter period of time compared with animals treated with IgG-APS and placebo. Hydroxychloroquine significantly diminished both thrombus size and total time of thrombus formation in mice previously injected with IgG-APS.
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                Author and article information

                Journal
                Journal ID (publisher-id): rmc
                Title: Revista médica de Chile
                Abbreviated Title: Rev. méd. Chile
                Publisher: Sociedad Médica de Santiago (Santiago, , Chile )
                ISSN (Print): 0034-9887
                Publication date (Print and electronic): August 2013
                Volume: 141
                Issue: 8
                Pages: 1041-1048
                Affiliations
                [01] Santiago orgnamePontificia Universidad Católica de Chile orgdiv1Departamento de Inmunología Clínica y Reumatología Chile gutierre@ 123456med.puc.cl
                Article
                Publisher ID: S0034-98872013000800011 Publisher ID: S0034-9887(13)14100800011
                DOI: 10.4067/S0034-98872013000800011
                SO-VID: 68c288ae-6e08-40be-9fc6-d5236efed475
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                Date received : 21 June 2012
                Date accepted : 09 October 2012
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 45, Pages: 8
                Product

                SciELO Chile

                Categories
                Subject: ARTICULOS DE REVISION

                Keywords: Therapies, investigational,Hydroxychloroquine, Hydroxymethylglutaryl-CoA Reductase Inhibitors,Antiphospholipid syndrome
                Data availability:
                Keywords: Therapies, investigational, Hydroxychloroquine, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Antiphospholipid syndrome

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